The surface of articular cartilage contains a progenitor cell population

Author:

Dowthwaite Gary P.1,Bishop Joanna C.1,Redman Samantha N.1,Khan Ilyas M.1,Rooney Paul2,Evans Darrell J. R.1,Haughton Laura1,Bayram Zubeyde3,Boyer Sam4,Thomson Brian4,Wolfe Michael S.5,Archer Charles W.1

Affiliation:

1. Cardiff School of Biosciences and Cardiff Institute of Tissue Engineering and Repair, Cardiff University, PO Box 911, Museum Avenue, Cardiff CF10 3US, UK

2. Tissue Services, National Blood Service, Langley Lane, Sheffield S5 7JN, UK

3. Department of Histology and Embryology, Akdeniz University, 070 Campus Antalya, Turkey

4. Smith and Nephew Group Research Centre, York Science Park, Heslington, York YO10 5DF, UK

5. Centre for Neurologic Diseases, Brigham and Women's Hospital and Harvard Medical School, 77 Avenue Louis Pasteur, Boston, MA 02115, USA

Abstract

It is becoming increasingly apparent that articular cartilage growth is achieved by apposition from the articular surface. For such a mechanism to occur, a population of stem/progenitor cells must reside within the articular cartilage to provide transit amplifying progeny for growth. Here, we report on the isolation of an articular cartilage progenitor cell from the surface zone of articular cartilage using differential adhesion to fibronectin. This population of cells exhibits high affinity for fibronectin, possesses a high colony-forming efficiency and expresses the cell fate selector gene Notch 1. Inhibition of Notch signalling abolishes colony forming ability whilst activated Notch rescues this inhibition. The progenitor population also exhibits phenotypic plasticity in its differentiation pathway in an embryonic chick tracking system, such that chondroprogenitors can engraft into a variety of connective tissue types including bone, tendon and perimysium. The identification of a chondrocyte subpopulation with progenitor-like characteristics will allow for advances in our understanding of both cartilage growth and maintenance as well as provide novel solutions to articular cartilage repair.

Publisher

The Company of Biologists

Subject

Cell Biology

Reference21 articles.

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4. Berezovska, O., Jack, C., McClean, P., Aster, J. C., Hicks, S., Xia, W., Wolfe, M. S., Kimberly, W. T., Weinmaster, G., Selkoe, D. J. et al. (2001). Aspartate mutations in presenillin and gamma-secretase inhibitors both impair notch 1 proteolysis and nuclear translocation with relative preservation of notch 1 signalling. J. Neurochem.75, 583-593.

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